Consumer acceptance of boar meat has been hindered by an objectionable odor in the heated fat of the meat from intact male pigs. Despite the fact that intact male pigs grow faster, utilize feed more efficiently and produce leaner carcasses, castration of male pigs grown for meat production has long been used in commercial practice to eliminate the undesirable odor referred to as "boar odor", "boar taint" or "male sex odor" in pork.
It is generally accepted in the prior art that a family of 5-.alpha.-C.sub.19 -16-en steroids (specifically 5-.alpha.-androst-16-en-3-one, 5-.alpha.-androst-16-en-3.alpha.-ol and 5-.alpha.-androst-16-en-3.beta.-ol) are responsible for the objectionable boar odor.
The 5-.alpha.-C.sub.19 -16-en steroids are synthesized in the boar testes by the metabolic pathway shown in FIG. 1 below: Brooks et at., J. Anim. Sci. 62 (1986) 632-645. ##STR1##
Further, Skatole, a metabolite formed during the breakdown of tryptophan by intestinal microorganisms in pigs, has been found to strengthen synergistically the unpleasand odor of 5-.alpha.-androst-16-en-3-one (Lundstrom, et al. Proc. European Meat. Res. Work 26:300 (1980).
Methods for preventing the formation of 5-.alpha.-C.sub.19 -16-en steroids in adult boars, thereby preventing the male sex odor in pork without the need for castration, have concentrated on environment rearing and autoimmunizing young boars against the 5-.alpha.-C.sub.19 -16-en steroids (Brooks, et al, J. Anim. Sci 62:632-645 (1986)). Thus far these methods have met with only limited success.
Antibiotics, such as virginiamycin, have demonstrated some efficacy in reducing the level of boar taint by lowering the levels of skatole. (Gadd, Pigs-Misset May/June (1992) p17).
With the exception of castration, no reliable method for preventing boar taint in adult male pigs is currently available.
One method of inhibiting boar taint which has to date received virtually no attention is the development of chemical agents which block the production of 5-.alpha.-C.sub.19 -16-en steroids.
Brophy and Gower (Biochem. Biophys. Acta 360:252) found that 5-.alpha.-pregnane-3,20-dione inhibits the andien-.beta. syntheses system, which is responsible for conversion of pregnenolone to 5, 16-androstadien-3.beta.-ol. However, practical use of 5-.alpha.-pregnane-3, 20-doine as an inhibitor of 5-.alpha.-C.sub.19 -16-en steroid formation is not feasible because it simultaneously inhibits formation of androgenic and estrogenic sex hormones elsewhere in the biosynthetic pathway of steroidal hormones in the boar. The use of chemical agents to prevent the conversion of 17.beta.-hydroxy-3-oxoandrost-4-ene to 17.beta.-hydroxy-5-.alpha.-androst-3-one by inhibiting the activity of steroid 5-.alpha.-reductase in rats, dogs and humans has been examined (Liang, et al. Endocrinology, 117, No. 2, 571-579 (1985)) (hereinafter Liang, et al.). Liang concluded that there are significant differences between the rat, dog and human forms of 5-.alpha.-reductase thereby emphasising the nontransferability of an agent's inhibitory potential of this enzyme between species. To date no successful method of chemically inhibiting the boar 4-ene-5-.alpha.-reductase enzyme, thereby preventing the in vivo conversion of 4,16-androstadien-3-one to 5-.alpha.-androst-16-en-3-one, has been reported.
The development of a suitable chemical-blocking agent to prevent formation of the boar 5-.alpha.-C.sub.19 -16-en steroids without inhibiting production of 4-ene androgenic and estrogenic sex hormones would be extremely valuable. Preferably such chemical-blocking agent will prevent the formation of 5-.alpha.-androst-16-en-3-one so that subsequent reduction to the .alpha.-ol and .beta.-ol forms are also prevented.